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Sp: Intro to Anes > 3. Premedication --> Maintenance of Anesthesia > Flashcards

3. Premedication --> Maintenance of Anesthesia Flashcards

1
Q

benzodiazepine drugs

A

midazolam (versed)
lorazepam
diazepam

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2
Q

benzodiazepine mechanism

A

binds to GABA receptor

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3
Q

benzodiazepine effects

A

anxiolysis
antegrade amnesia
anticonvulsant
minimal cardiac/resp depression

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4
Q

benzodiazepine reversal agents

A

flumazenil (Romazicon)

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5
Q

benzodiazepine side effects

A

increased apnea
increase risk of post-op cognitive dysfunction

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6
Q

midazolam administration

A

IV
PO
intranaal

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7
Q

midazolam IV dose

A

1-2mg

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8
Q

midazolam PO (peds)

A

0.3-0.7 mg/kg
up to 20mg

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9
Q

midazolam intranasal dose

A

0.2-0.5mg/kg

causes nasal burning

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10
Q

midazolam onset IV

A

rapid
20-25 secs

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11
Q

midazolam onset PO

A

10-15 min

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12
Q

midazolam onset intranasal

A

5-10 min

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13
Q

Pre-Induction Checklist

A

Machine
Suction
Monitors
Airway (+emergency devices)
Invasive lines
Drugs
Special items

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14
Q

most common methods for inducing pt

A

IV
Mask
IM (ketamine dart)

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15
Q

fresh gas flow (FGF)

A

how fast gas is flowing
(L/min)

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16
Q

Inspiratory concentration factors
(Fi)

A

Fresh gas flow
breathing circuit volume
circuit absorption of agent

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17
Q

when machine absorbs a high amount of agent…

A

the pt absorbs less agent

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18
Q

FGF and Fi relationship

A

directly proportional

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19
Q

FGF and circuit volume relationship

A

???

increase volume decrease delivery?

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20
Q

alveolar concentration factors
(FA)

A

uptake (into blood)
minute ventilation
overpressurization

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21
Q

we want FA to ______

A

increase as quickly as possible

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22
Q

uptake (into blood)

A

incr uptake decr partial pressure

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23
Q

uptake factors

A

blood:gas coefficient
pulmonary blood flow
difference in alveolar gas and blood

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24
Q

blood: gas coefficient

A

tells us how soluble an agent is in the blood

more soluble = more uptake
= slower FA increase

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25
Q

high B:G

A

slower FA increase

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26
Q

low B:G

A

faster FA increase

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27
Q

pulmonary blood flow

A

decreased CO = decreased uptake
= faster FA

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28
Q

agent concentration in alveolar gas vs venous blood

A

want higher [agent] in aveoli vs blood
generates larger driving force

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29
Q

N2O B:G

A

0.47

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30
Q

Iso B:G

A

1.4

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31
Q

Des B:G

A

0.42

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32
Q

Sevo B:G

A

0.65

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33
Q

minute ventilation and FA relationship

A

increased minute ventilation replaces anesthetic taken up into pulmonary

we want higher minute ventilation

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34
Q

overpressurization effect

A

increase amt of agent inspired (Fi)
increase Fi = increased downstream concentration

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35
Q

Fi vs FA

A

increasing Fi leads to a greater increase FA

5x Fi = 6.2x FA

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36
Q

augmented inflow effect

A

add gas to replace absorbed agent

Patm > Palveoli
sucks gas into alveoli (high – > low)

5xFi = 6.8x FA

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37
Q

second gas effect

A

soluble first gas (N2O) is given at high inspired concentrations

N2O leaves alveoli quickly
causes over pressurization of sevo
increases driving factor
==faster induction

the partial pressure of the gas left behind (sevo) is relatively greater than that of the remaining gases (over pressurization)

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38
Q

Arterial concentration (Fa) factors

A

Ventilation-Perfusion mismatch (V/Q)

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39
Q

ventilation-perfusion mismatch
(V/Q)

A

mismatched distribution of ventilation / perfusion of lung units
some receiving high ventilation
others receiving high perfusion

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40
Q

V/Q results in

A

alveolar dead space
incr deadspace
== decr induction speed

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41
Q

Procedures that may cause V/Q

A

bronchial intubation
R-L shunt

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42
Q

MAC

A

the end-tidal concentration necessary to prevent movement in 50% of pts

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43
Q

1.3 MAC

A

prevents movement in 95% of surgical pts

(1.2-1.3 MAC)

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44
Q

0.5 Nitrous + 0.5 Sevo =

A

1.0 MAC
MAC is additive

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45
Q

MAC-awake

A

end tidal concentration that allows pt to respond meaningfully to stimuli

0.3-0.5 MAC

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46
Q

MAC-Awake (N2O)

A

0.64 MAC

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47
Q

MAC - Amnesia

A

concentration to prevent recall in 50% of pts
0.25-0.4 MAC (up to 0.6)

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48
Q

MAC-BAR

A

concentration where 50% of population wont mount an adrenergic response

1.5-1.6 MAC

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49
Q

N2O MAC

A

105%

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50
Q

ISO MAC

A

1.2%

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51
Q

DES MAC

A

6.0%

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52
Q

SEVO MAC

A

2.0%

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53
Q

MAC and age relationship

A

inversely proportional

young age = higher MAC

54
Q

N2O supports…

A

combustion

N2O –> 2N2 + O2

55
Q

what gas agent does not trigger MH

A

N2O

56
Q

N2O cardiovascular response

A

sympathomimetic
no change to HR (slight evelation)

57
Q

N2O respiratory response

A

increase RR
decrease TV
increase PVR (pulm vasc. resistance)

58
Q

N2O mechanism

A

NMDA receptor antagonist
may provide analgesia bc NMDA is involved in pain transmission

59
Q

N2O contraindications

A

N2O will expand air filled spaces

60
Q

Sevo properties

A

nonflammable
non-pungent

61
Q

Sevo CV effects

A

decrease contractility
decrease SVR
decrease BP
no change HR

62
Q

Sevo respiratory effects

A

increase RR
decrease TV
bronchodilator

63
Q

Sevo cerebral effects

A

increase CBF
increase ICP
decrease CMRO2 (brain O2 consum)

64
Q

Sevo and MH

A

triggers MH

65
Q

Sevo metabolism

A

5% metabolized
flouride metabolite - nephrotoxicity

66
Q

Compound A

A

produced by interactions w/Sevo and the barium hydroxide lime/soda lime
nephrotoxic

2LPM flow rate for sevo gas

67
Q

Isoflurane properties

A

nonflammable

68
Q

Iso CV effects

A

decrease contractility
decrease
SVR
decrease BP
increase HR
maintains CO (cardiac output)
vasodilation

69
Q

Iso Respiratory effects

A

increase RR
decrease TV
bronchodilation

70
Q

Iso Cerebral effects

A

increase CBF
increase ICP
decrease CMRO2

71
Q

ISO and MH

A

triggers MH

72
Q

coronary steal

A

Pt has blocked CA == vasodilation

if you give Iso:
Iso causes vasodilation of other arteries which “steal” blood from the blocked CA

73
Q

Des properties

A

non-flammable
pungent airway irritant
20C vapor pressure = 681mmHg
(special vaporizer)

74
Q

Des CV effects

A

increase HR
decrease SVR
decrease BP
maintain CO

75
Q

Des respiratory effects

A

increase RR
decrease TV
bronchoconstriction (asthmatic pts)

76
Q

Des cerebral effects

A

increase CBF
increase ICP
decrease CMRO2

77
Q

Des and MH

A

triggers MH

78
Q

how do we choose volatile agent?

A

type of surgery
cost/availability
fat:blood ratio
pt characteristics

79
Q

N2O F:B

A

2.3

80
Q

Iso F:B

A

45

81
Q

Des F:B

A

27

82
Q

Sevo F:B

A

48

83
Q

why IV induction more common?

A

rapidly bypass stage 2
rapid recovery after bolus dose due to redistribution to tgt site
more portable
not greenhouse gases

84
Q

Propofol mechanism

A

GABAa receptor agonist

85
Q

propofol onset

A

rapid

86
Q

Propofol duration of action

A

short
why?

87
Q

Propofol expiration

A

6 hrs post opening

88
Q

Propofol CV

A

decrease BP
decrease SVR
decrease preload
decrease contractilioty

89
Q

Propofol Respiratory

A

profound resp depression
depresses upper airway reflexes

90
Q

Propofol Cerebral

A

decrease CBF
decrease ICP
decrease CMRO2
anticonvulsant (incr seizure thresh)
myoclonic movement

91
Q

Proprofol misc effects

A

histamine release
antiemetic

92
Q

Ketamine Mechanism

A

NMDA antagonist

93
Q

Ketamine main effect

A

dissociative anesthesia
- diss sensory impulses from limbic cortex
- limbic system: awareness of sensation/emotions

94
Q

Ketamine administration

A

IV
IM
Oral
Nasal
Rectal

low dose infusion for pain

95
Q

Ketamine IV Onset/DOA

A

Onset: rapid
DOA: 5-10 min

96
Q

Ketamine CV

A

incr BP
incr HR
incr CO
incr myocardial O2 demand
central sympathetic stimulant
(direct myocardial depressant)

97
Q

Ketamine respiratory

A

no resp depression
bronchodilation
intact airway reflexes/muscle tone

98
Q

Ketamine cerebral

A

incr CBF
incr ICP
incr CMRO2

99
Q

Ketamine side effects

A

psychotomimetic (dreams/delirium)
seizures at low dose
anticonvulsant at high dose
incr secretions

100
Q

Etomidate mechanism

A

GABA receptor agonist
depresses reticular activating system
(RAS)
- regulates sleep/arousal

101
Q

Etomidate Onset

A

rapid

102
Q

Etomidate metabolism

A

hepatic
plasma esteraseE

103
Q

Etomidate side effects

A

PONV
myoclonus (30-60%)
injection pain
adrenal suppression (24-48 hrs post)

104
Q

Etomidate CV effects

A

minimal

105
Q

Etomidate Respiratory effects

A

mild resp depression

106
Q

Etomidate Cerebral effects

A

decr CBF
decr ICP
decr CMRO2
maintains CPP (perfusion pressure)
increases SSEP amplitude (TOF?)
seizure potential

107
Q

Lidocaine induction uses

A

reduce propofol burning
blunt airway response to DL

1mg/kg IV

108
Q

Most common analgesic

A

fentanyl

109
Q

fentanyl properties

A

fast acting
fat soluble =
crosses plasma membrane
long half life

110
Q

Neuromuscular blocking agents

A

depolarizing
non-depolarizing

111
Q

Succinylcholine mechanism

A

depolarizing

attached to ACh receptor causing random fasiculations and eventual paralysis

112
Q

Sux onset/DOA

A

onset: 45 sec (IV)
duration: 10 min

113
Q

Sux reversal

A

no reversal needed due to rapid recovery

114
Q

Sux metabolism

A

plasma psuedocholinesterase

(butyrylcholinesterase)

115
Q

Sux myalgia treatment

A

can treat w/ROC
(0.06-0.1 mg/kg IV)

116
Q

Sux CV effects

A

bradycardia
(stimualtes cardiac postgang muscarinic receptors)

117
Q

Sux and MH

A

triggers MH

118
Q

Sux Contraindication

A

muscular dystrophy
– sux can trigger rhabdo

hyperkalemia
–sux can incr [K+] by 0.5
– burns/trauma
–spinal cord injuries
–sepsis

119
Q

Pseudocholinesterase deficiency

A

AKA atypical plasma cholinesterase
AKA atypical Butyrylcholinesterase

genetic abnormality in psuedocholinesterase gene

120
Q

Heterozygous atypical
pseudocholinesterase deficiency

A

20-30min blockade duration
dibucaine #: 40-60

121
Q

Homozygous atypical
pseudocholinesterase deficiency

A

60min-8hr blockade duration
dibucaine #: 20-30

122
Q

dibucaine number

A

test for pseudocholinesterase def
measures function not amount

less inhibitory to genetic changes
(homo: lower number)
(hetero: higher number)
(not mutated: highest)

123
Q

Non-Depolarizing NMB categories

A

benzoisquinolone
steroidal
chlorofumarate

124
Q

benzoisquinolone NMB drugs

A

cisatracurium

125
Q

steroidal NMB drugs

A

vecuronium
rocuronium

126
Q

chlorofumarate NMB drugs

A

gantacurium (experimental)

127
Q

rocuronium onset/duration

A

onset: 60-90s
duration: 35-75 min

128
Q

roc elimination

A

mostly biliary
some kidney
- not prolonged by kidney failure

129
Q

vecuronium onset/duration

A

onset: 2-3 min
duration: 45-90 min

130
Q

vec elimination

A

mostly biliary (small hepatic)
25% kidney
- mod prolong by kidney failure

131
Q

cisatracurium onset/duration

A

onset: 2-3 min
duration: 40-75 min

132
Q

cisatracurium elimination

A

hoffman elimination
- laudanosine metabolite

**use with kidney/liver failure pts
pH/temp sensitive drug

Sp: Intro to Anes (12 decks)

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